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OBM Neurobiology

(ISSN 2573-4407)

OBM Neurobiology is an international peer-reviewed Open Access journal published quarterly online by LIDSEN Publishing Inc. By design, the scope of OBM Neurobiology is broad, so as to reflect the multidisciplinary nature of the field of Neurobiology that interfaces biology with the fundamental and clinical neurosciences. As such, OBM Neurobiology embraces rigorous multidisciplinary investigations into the form and function of neurons and glia that make up the nervous system, either individually or in ensemble, in health or disease. OBM Neurobiology welcomes original contributions that employ a combination of molecular, cellular, systems and behavioral approaches to report novel neuroanatomical, neuropharmacological, neurophysiological and neurobehavioral findings related to the following aspects of the nervous system: Signal Transduction and Neurotransmission; Neural Circuits and Systems Neurobiology; Nervous System Development and Aging; Neurobiology of Nervous System Diseases (e.g., Developmental Brain Disorders; Neurodegenerative Disorders).

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Open Access Review

Mycotoxins Exposure: Neuroinflammation, Cognitive Decline and Behavioral Alteration

Mojtaba Ehsanifar 1,* ORCID logo, Akram Gholami 2, Joseph P Reiss 3

  1. Department of Environmental Health Engineering, School of Medical Sciences, Torbat Jam Faculty of Medical Sciences, Torbat Jam, Iran

  2. Department of Nursing, School of Medical Sciences, Torbat Jam Faculty of Medical Sciences, Torbat Jam, Iran

  3. Director of Environmental Sciences at Certified Site Safety of New York, LLC, and International Institute of Environmental and Medical Studies, NJ, United State

* Correspondence: Mojtaba Ehsanifar ORCID logo

Academic Editor: Fabrizio Stasolla

Received: June 13, 2025 | Accepted: October 14, 2025 | Published: October 21, 2025

OBM Neurobiology 2025, Volume 9, Issue 4, doi:10.21926/obm.neurobiol.2504305

Recommended citation: Ehsanifar M, Gholami A, Reiss JP. Mycotoxins Exposure: Neuroinflammation, Cognitive Decline and Behavioral Alteration. OBM Neurobiology 2025; 9(4): 305; doi:10.21926/obm.neurobiol.2504305.

© 2025 by the authors. This is an open access article distributed under the conditions of the Creative Commons by Attribution License, which permits unrestricted use, distribution, and reproduction in any medium or format, provided the original work is correctly cited.

Abstract

Evidence from recent studies has suggested a significant association between mycotoxin exposure and neuroinflammation, potentially contributing to the onset of neurocognitive disorders during key developmental stages of the brain. Various research highlights how exposure to these toxins is correlated with a decline in cognitive performance, reduced motor skills, and behavioral issues. Mycotoxins are also implicated in interfering with neuronal signaling pathways and the functioning of neurotransmitters, which may lead to neurodevelopmental disorders. This review aims to synthesize existing literature on the link between mycotoxins and neuroinflammatory responses, brain maturation, and cognitive deficits, whilst identifying potential areas for future research endeavors.

Keywords

Mycotoxin exposure; neuroinflammation; neurodevelopmental disorders; cognitive impairments

1. Introduction

Mycotoxins are secondary metabolites naturally produced by certain types of fungi. These toxins can contaminate food and food products, and humans can be exposed by eating contaminated items or consuming animal products like milk, meat, and eggs from animals fed on contaminated feed [1,2]. Children are particularly susceptible to mycotoxin exposure, mainly because they often consume snacks and foods made from grains that may contain these toxins. Due to their higher metabolic rates and less developed detoxification systems, infants, toddlers, and young children are more prone to the harmful effects of mycotoxins. This is crucial as it can negatively impact their brain development and overall health. The development of the brain is a highly complex process beginning shortly after fertilization and extending into adulthood. The activities involved in this development include the birth of cells (neurogenesis, gliogenesis), differentiation, maturation (involving dendrites and axons), migration, synapse creation (synaptogenesis), myelin formation (myelogenesis), synaptic pruning, and ultimately, cell death [3]. Significant aspects of a child's development—such as movement, language, social interactions, and cognitive abilities—are all deeply rooted in brain development. Early childhood is a crucial time for establishing the neural connections essential for brain function. During these years, neural networks rapidly formed. The cholinergic systems, critical for brain processing, have their origins during the initial stages of central nervous system (CNS) development [4]. Variations in dopamine pathways also disrupt significant neural development processes such as migration, differentiation, and synaptogenesis [5]. Proper nutrition during the first three years of life is vital for brain growth and neural development [6,7]. Healthy brain development hinges on adequate care and nutrition in infancy [8]. Neurodevelopmental disorders, which manifest during the developmental phase, can lead to functional impairments. These include attention deficit/hyperactivity disorder (ADHD), autism spectrum disorders, intellectual disabilities, learning challenges, cerebral palsy, conduct disorders, sensory impairments, motor disorders like tic conditions, and specified learning issues [9]. Although prevalent in younger populations, these disorders may persist or remain undiagnosed into adulthood [10]. The precise causes of these disorders remain unclear, but exposure to neurotoxins during key developmental phases can disrupt brain functions and connectivity, potentially leading to neurodevelopmental disorders. Children, with their ongoing brain development and limited ability to metabolize harmful substances, are particularly vulnerable to mycotoxins, which may contribute to these disorders [11]. Dietary mycotoxins are associated with increased risks of disorders such as autism [12,13,14], and they are perceived as common foodborne toxins. Some mycotoxins can breach the blood-brain barrier, affecting normal CNS operations [15,16]. These toxins exhibit neurotoxic properties that might induce neurodevelopmental disorders by impacting neurotransmitter systems, neuronal activities, immune responses, and the nervous system. Mycotoxins also contribute to oxidative stress by producing free radicals, leading to membrane and cell damage. Moreover, they can inflict brain damage through infections caused by astrocytes and microglia [5,17], highlighting the critical need to address mycotoxin exposure in safeguarding health, particularly during vital stages of brain development.

2. Factors Affecting Mycotoxin Contamination

Several elements contribute to the contamination of mycotoxins, beyond nutrition alone. Environmental factors, climate change implications, socio-economic conditions, and agricultural aspects influence it. Notably, high humidity and high temperatures, combined with socioeconomic challenges and suboptimal storage techniques for food and farming goods, significantly raise the risk of mycotoxin presence [18,19]. Environmental Factors: High humidity and temperatures are recognized as the primary triggers for fungal growth and mycotoxin contamination during both the pre-harvest and post-harvest phases of agricultural products [20]. Climate Change Implications: Alterations in climate are likely to worsen mycotoxin issues. Predictions underscore that shifts in temperature, water availability, and humidity levels will enhance conditions for mycotoxin-producing fungi [21]. Socio-Economic Conditions: Poor socioeconomic conditions, such as residing in homes with excessive humidity and inadequate ventilation, along with ineffective agricultural practices, aggravate the growth of fungi [22]. These factors exacerbate mycotoxin prevalence, especially within regions like sub-Saharan Africa, which is most affected by these challenges. Addressing these factors may help mitigate the risks posed by mycotoxin contamination.

3. Mechanisms of Mycotoxin-Induced Brain Damage

Mycotoxins inflict brain damage through various pathways, including disrupting the blood-brain barrier (BBB), generating oxidative stress, inciting neuroinflammation, causing DNA damage, inducing apoptosis, and impeding neurogenesis, as well as leading to mitochondrial dysfunction [23]. Researchers have cataloged over 300 distinct mycotoxins, some exhibiting neurotoxic properties [16]. Mycotoxins impair BBB integrity via several mechanisms, including oxidative stress and matrix metalloproteinase-9 (MMP-9) activation [24]. The compromised BBB permits mycotoxins in the bloodstream to access the brain, impacting nervous system functions [25,26]. Aflatoxins can readily traverse the BBB, disrupting brain immune defenses [15,17]. Exposure to fumonisins diminishes the expression of P-glycoprotein, a transporter protein responsible for expelling toxins and foreign materials from the brain. Lower P-glycoprotein levels can increase harmful substance accumulation in the brain, exacerbating neural tissue damage [27,28]. Substances like T-2 toxin and deoxynivalenol heighten BBB permeability by damaging BBB integrity and impairing endothelial cell function [29]. The CNS acts as a wiring system, transmitting data electrically and chemically through neurotransmitter-released nerve cell networks. These chemical signals affect other cells' functions. Mycotoxins can interfere with these signals if their structures resemble neurotransmitter precursors or receptors, like ergot alkaloids, acting as enzyme substrates involved in conversion [30,31]. Increased dopamine metabolism is observed after exposure to AFB1 [32], deoxynivalenol [33], or fumonisins, suggesting a compensatory mechanism for regulating neurotransmitter levels or enhanced synaptic dopamine release [32]. AFB1 hampers inhibitory neurotransmitter function, reducing cation influx into neurons and disrupting ion balance [34]. AFB1, HT-2 toxin, and T-2 toxin disrupt tryptophan metabolism, hindering serotonin synthesis and metabolism, thereby lowering brain serotonin levels [32]. GABA, a neurotransmitter found in 30–40% of all CNS neurons, may be affected by mycotoxin exposure, leading to inhibited GABA synthesis [30]. In addition, OTA affects calcium-dependent signaling pathways critical for neurotransmitter release and synaptic plasticity [35]. Mycotoxin exposure impairs cholinergic neurotransmission by inducing an imbalance between acetylcholinesterase (AChE) and acetylcholine in the brain, thereby affecting cognitive functions, memory, and learning [36,37].

Mycotoxins impair mitochondrial function through oxidative stress by generating reactive oxygen species (ROS), causing neurotoxicity in the CNS. Oxidative stress, detrimental to the brain, leads to numerous neurological disorders. Mycotoxins exert an indirect effect on immune system activation, primarily interacting with phagocytic cells and immune responses [38,39].

Oxidative stress alters intracellular antioxidant systems (e.g., glutathione peroxidase, superoxide dismutase, catalase, nuclear factor erythroid-related 2 [Nrf2]), impacting oxidative stress-related gene expression [40,41,42] and activating apoptosis and DNA damage pathways, contributing to neuronal dysfunction [43,44]. Mycotoxins initiate apoptosis by activating caspases, such as caspase-8, 9, and 3 [28,45], liberating cytochrome c and apoptosis-inducing factors (AIF) from mitochondria, and altering the expression of apoptotic regulators [40,46]. An additional significant mechanism, mitochondrial dysfunction [47,48], impedes the nervous system's energy availability by affecting adenosine triphosphate (ATP) regulation, the primary cellular energy source, and impacting calcium homeostasis, which involves endoplasmic reticulum membrane disruption and lipid peroxidation escalation [17]. This disruption stems from mitochondrial metabolic blockade of the electron transport chain's complex I, thereby affecting neuronal growth [49]. Oxidative stress also hampers cholinergic synapse and neuromuscular junction neurotransmission by inhibiting AChE [50].

Mycotoxins, inducing inflammatory responses, stimulate cytokine production, such as interleukins 1β and 6 (IL-1β and IL-6) and tumor necrosis factor-β (TNF-β), nitric oxide (NO), and inducible NO synthase (iNOS), enhancing chemokine generation in the brain [38]. Furthermore, mycotoxins initiate neuroinflammation within microglial cells by activating NLRP3 via various signaling pathways [51]. Excessive cytokine production by mycotoxins can incite chronic and damaging inflammatory events, affecting BBB integrity, with systemic cytokines intensifying CNS inflammation [52,53]. Mycotoxin-induced neuroinflammation leads to gliosis or astrocyte and glial cell proliferation, which increases the incidence and severity of CNS infections due to its effects on systemic immunity, especially with significant mycotoxin exposure [54].

4. Neurotoxicity Associated with Mycotoxin Exposure

Mycotoxins can be encountered through various pathways: ingestion, inhalation, or skin contact. Studies reveal significant connections between mycotoxin exposure during prenatal and postnatal periods and various adverse outcomes related to neurodevelopment. These include disturbances in sensory, motor, and cognitive skills, and an increased risk of developing neurodevelopmental disorders, such as autism spectrum disorders [55,56].

Exposure to mycotoxins, particularly during key stages of brain growth, can result in lasting and irreversible neurological conditions, including learning disorders and cognitive impairments. The detrimental effects of mycotoxins are primarily due to their interaction with mitochondria, which triggers an overproduction of ROS and leads to compromised mitochondrial functions. Generally, mycotoxin exposure is linked to harmful impacts on brain development and neurological health [13,57].

Epidemiological research has recorded a rise in certain neurological disorders linked with environmental influences, such as mycotoxin-laden food consumption, in children. Disorders like attention deficit disorder, autism, intellectual disability, and learning disabilities, among others, are cited [13]. A noteworthy cross-sectional study comparing Italian children with autism to those not affected showed heightened vulnerability to negative results in autistic children exposed to mycotoxins, underlining the dual risk posed by mycotoxins in these children [58]. Another study highlighted increased levels of ochratoxin A—a type of mycotoxin—in the blood and urine samples of autistic children, versus their healthy counterparts, suggesting ochratoxin A's significance in children with autism spectrum disorder (ASD) [13]. However, further research by Duringer et al. contradicted these findings by not establishing a link between ochratoxin A and ASD in children [59]. Investigations into mycotoxins' effects on children's brain development typically rely on behavioral assessments, neurophysiological testing like electroencephalography or magnetoencephalography, or advanced imaging techniques such as structural or functional MRI scans. Most knowledge regarding mycotoxin exposure and brain development stems from animal research. In human studies, assessing mycotoxin effects on the brain is challenging due to difficulties in measuring mycotoxins or related biomarkers, such as protein or DNA compounds and glucuronide conjugates. These measurements play a crucial role in linking mycotoxins to health outcomes. Analysis of mycotoxin biomarkers or metabolites is often conducted in urine, blood, or breast milk samples to ascertain the mycotoxin intake levels [11,13].

5. Investigating the Mechanisms and Effects of Mycotoxins on the Brain in Animal Models

Utilizing animal models is vital when monitoring health, as they help evaluate behavioral shifts in animals. For studying the neurotoxic effects of mycotoxins, both in vivo and in vitro methods are often employed. In vitro models typically involve examining the impact of mycotoxins on cell lines or tissues, providing essential details on cellular mechanisms of neurotoxicity. Conversely, in vivo models focus on assessing the effects of mycotoxins in living subjects, usually animals, offering a well-rounded view of mycotoxins' systemic impacts and organ system interactions. Rodents, notably mice and rats, are the primary laboratory models due to their significant genetic and physiological resemblance to humans and their sophisticated nervous systems. They are extensively utilized in neuroscience studies of neurotoxicity to evaluate neurodevelopment and behavior [60]. Apart from rodents, zebrafish, piglets, and the nematode Caenorhabditis elegans are also used in in vivo studies [30,34,61,62].

In specific in vivo models, the neurotoxic effects of mycotoxins are assessed through changes in behaviors such as motor skills, exploratory activities, learning, memory, anxiety, depressive symptoms, and reactions like object recognition, pain, and feeding behavior [63]. Studies report that mycotoxins like aflatoxin B1 and fumonisin B1 create considerable threats to the central nervous system, exacerbating behavioral issues and cognitive as well as neurological disorders. Animals are exposed to mycotoxins through naturally contaminated feed, oral gavage, or intraperitoneal injection, facilitating the analysis of neurotoxicity. These exposures lead to diminished antioxidant capabilities, increased pro-inflammatory cytokines, and changes in neurotransmitters and enzymes, triggering behavioral variations post-mycotoxin exposure [64,65,66]. Links between behavioral deficits such as impaired cognition and learning, anxiety-like behaviors, and motor dysfunction with synaptic dysfunction and changes in acetylcholine levels have been established [32,67]. Histopathological damage from mycotoxins is evident in observations such as reduced brain size, decreased nerve fibers, and neuron damage in various brain areas [68]. Exposure may also stimulate neurotransmitters in the brain, leading to anxiety-like behaviors and impairments in cognition, learning, and motor functions, affecting various brain structures and tissue [37,67,69]. The mechanisms through which mycotoxins cause brain damage relate to their capacity to breach the BBB. Damage to the BBB can result in behavioral changes such as depressive and anxiety-like symptoms [15]. Our previous research showed that environmental pollutants such as Chemical compounds [70] and pesticides [71,72], airborne aerosols [73] and nanoparticles [74], nanoplastics [75], and the ability to cross the BBB and induce oxidative stress and neuroinflammation can contribute to changes in cytokine gene expression, histological changes, behavioral changes [76], and impairments in memory, learning [77], anxiety, and depression [78] in mice. Oxidative stress induced by mycotoxins in animal models occurs through the production of ROS and diminished antioxidant defenses like catalase and glutathione reductase. These factors, which, through glial cell activation and pro-inflammatory cytokine secretion like TNF-alpha and interleukins, lead to brain harm and behavioral alterations [64,79,80,81], are significant contributors to neuroinflammation. Mitochondrial dysfunction might also cause damage to cellular lipids, proteins, and DNA through ROS production, with subsequent apoptosis triggered by specific apoptotic signaling pathways [82].

6. Potential Interventions to Reduce the Adverse Effects of Mycotoxins

Mycotoxin exposure poses a significant global risk, and there is still no definitive solution to eliminate it. Therefore, adopting methods to minimize exposure to these harmful substances is of paramount importance. Physical methods can be instrumental in eliminating contaminated grains from cereal products. While these techniques are successful in diminishing the intake of food products tainted by mycotoxins, they do not tackle the underlying issue of the fungal production of these toxins [83]. It's particularly concerning that children, due to their developing bodies, are highly vulnerable to mycotoxin exposure, which can lead to negative impacts on brain development. The repercussions of mycotoxin exposure in children manifest as decreased academic performance and reduced school effectiveness, potentially causing significant societal losses in future generations [19,84].

In nations with adequate resources, reducing the intake of mycotoxin-contaminated food is achievable by setting regulatory limits on mycotoxin levels in both food and feed. The European Union has imposed such limits on numerous mycotoxins. Similarly, the Codex Alimentarius has established standards but only for a limited range of mycotoxins across a few commodities. Nonetheless, several countries have yet to set these limits and continue to strive towards minimizing mycotoxin exposure [85].

7. Future Directions and Research Gaps

Reported associations include structural and functional changes in the brain in animal models and emerging human data, although causal associations and mechanisms are not fully elucidated. Understanding the mechanistic pathways and cellular and molecular mechanisms (e.g., oxidative stress, mitochondrial dysfunction, neuroinflammation, impaired calcium signaling) is essential. It is also vital to examine dose-response relationships and time periods of exposure (prenatal, early childhood, adolescence) that are most vulnerable to structural changes. Our previous studies have examined the effects of toxin exposure on oxidative stress and neurotoxicity [71] as well as the impact of environmental chemicals on mental health [70], but it is recommended to study interactions with nutritional status, co-exposure to mycotoxins with other environmental toxins and their effects on neurological disorders, and genetic susceptibility such as polymorphisms in detoxification enzymes. It would also be helpful to conduct longitudinal human MRI studies to track brain volume, cortical thickness, white matter integrity (DTI measures such as FA and MD), and connectivity changes in relation to quantitative mycotoxin exposure, and to investigate the effects of environmental exposure using multimodal imaging combining structural MRI with functional MRI (resting-state and task-based) to link structural changes to functional changes, as well as to develop standardized imaging biomarkers for brain changes associated with mycotoxin exposure to allow for cross-study comparisons, or to integrate environmental monitoring (food contamination data) with the investigation of the effects of individual exposures and imaging outcomes.

8. Conclusion

In conclusion, Mycotoxin exposure during vital stages of brain growth might trigger neurocognitive issues like diminished cognitive abilities, motor skill challenges, and behavioral irregularities. By interfering with neural messaging and neurotransmitter anomalies, mycotoxins are likely to play a role in developmental disorders such as ADHD, autism, intellectual impairments, learning disorders, and cerebral palsy. It's crucial to devise methods for reducing mycotoxin contamination in consumables and to improve public knowledge about the dangers associated with mycotoxin exposure. Safeguarding children from the negative impacts of mycotoxins on neurological development is vital. Ensuring the safety of food sources and minimizing mycotoxin exposure is of utmost importance. Continued studies could shed light on the specific neurotoxic consequences of mycotoxins on brain disorders. Further studies are needed to investigate how mycotoxins affect neural development and to develop practical solutions for maintaining brain health.

Acknowledgments

We thank Dr. Ehsanifar Research Lab. Tehran, Iran.

Author Contributions

Dr. ME Conceptualization, Supervision and Writing – original draft – review & editing; AG and JPR Writing – review & editing. All the authors contributed to writing, reviewing and editing and agreed to the published version of the manuscript.

Funding

This review received no external funding and was initiated and funded by Dr. Ehsanifar Research Lab, Tehran, Iran.

Competing Interests

The authors declare that they have no competing interests.

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